Key result
CTLA-4 inhibition preferentially results in giant cell myocarditis with a predominately CD4+ T cell infiltrate, whereas PD-1 inhibition leads to lymphocytic myocarditis with a predominately CD8+ T cell infiltrate.
Why the study?
Immune checkpoint inhibitors cause immune-related adverse events such as myocarditis, and distinct ICI targets appear to precipitate specific myocardial infiltrates including lymphocytic or giant cell myocarditis.
This review highlights that different immune checkpoint inhibitors precipitate distinct forms of myocarditis, suggesting that tailored immunosuppressive strategies targeting specific T cell pathways may be required.
May support ICI-specific immunosuppression; leaves open prospective validation of tailored regimens.
The advent of immune checkpoint inhibitors (ICIs) has revolutionized the field of oncology, but these are associated with immune related adverse events. One such adverse event, is myocarditis, which has limited the continued immunosuppressive treatment options in patients afflicted by the disease. Pre-clinical and clinical data have found that specific ICI targets and precipitate distinct myocardial infiltrates, consistent with lymphocytic or giant cell myocarditis. Specifically, it has been reported that CTLA-4 inhibition preferentially results in giant cell myocarditis with a predominately CD4+ T cell infiltrate and PD-1 inhibition leads to lymphocytic myocarditis, with a predominately CD8+ T cell infiltrate. Our manuscript discusses the latest literature surrounding ICI pathways and targets, while detailing proposed mechanisms behind ICI mediated myocarditis.
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Rikhi et al. (2021) conducted a review in Immune checkpoint inhibitor-mediated myocarditis. Immune checkpoint inhibitors was evaluated. CTLA-4 inhibition preferentially results in giant cell myocarditis with a predominately CD4+ T cell infiltrate, whereas PD-1 inhibition leads to lymphocytic myocarditis with a predominately CD8+ T cell infiltrate.
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